糖尿病小型猪心肌、肝脏组织结构变化和心肌VEGF表达

以探讨高糖高脂高胆固醇饲料诱发的糖尿病广西巴马小型猪心肌和肝脏组织结构变化、肝糖原分解和心肌血管内皮生长因子(VEGF)表达情况为目的.通过3月龄雄性广西巴马小型猪10只,随机分2组,5只饲以基础饲料为CD组;5只饲以高糖高脂饲料为HFSCD组,饲养时间5个月.每月末从禁食过夜的小型猪眶静脉窦抽取血样,葡萄糖氧化酶法检测空腹血糖(Glucose);GPO-PAP酶法测定血浆甘油三脂(triglyceride,TG);放射免疫法测血浆胰岛素.第5个月末股动脉放血处死小型猪,取1小块心肌和肝脏组织,固定于10%中性甲醛固定液,常规石蜡包埋、切片、制片后用光学显微镜进行观察的方法.结果HFSCD组血糖、甘油三酯和胰岛素水平升高.与CD组比较,差异具有显著性意义(P<0.05).从肝脏病理切片观察所见,HFSCD组肝脏肝细胞索排列紊乱,肝细胞肿胀呈气球样变,亦可见肝细胞萎缩、坏死,脂肪变性明显,肝小叶间有单个核细胞浸润,肝糖原极少或消失.心肌组织中VEGF的蛋白表达显著增加,且表达范围广泛.得出高糖高脂高胆固醇饲料诱发的糖尿病广西巴马小型猪肝脏和心肌组织结构改变,肝糖原减少,心肌VEGF蛋白表达增加的结论.图5,参13.     

六价铬化合物的肝脏毒性及其作用机制研究进展

六价铬化合物普遍存在于环境中,并被广泛应用于多种工业生产中,由此引发的铬污染及健康问题已经引起了人们的重视。作为体内代谢及解毒的重要场所,肝脏是Cr(Ⅵ)毒性作用的靶器官之一。本文对Cr(Ⅵ)化合物在环境中的污染来源与污染状况、机体内吸收、分布与代谢及对肝脏的毒性损害及其作用机制的研究现状加以综述。     

Alpha-tocopherol supplementation on chromium toxicity: a study on rat liver and kidney cell membrane

Membrane damage is one of the important consequence of chromium,an environmental toxicant,to produce cytotoxicity.α-tocopherol,a membrane protectant can be used to reduce the chromium-induced membrane damage.In the present study,the impact of chromium in presence and absence of α-tocopherol was studied on plasma membrane of live and kidney in male Wistar rats(80-100g body weight).Significant increase in membrane cholesterol level as well as significant decrease in membrane phospholipid level in chromium exposed(0.8mg/100g body weight/d,i.p.,for 4 weeks)animals suggest structural alteration of both liver and kidney plasma memebrane.The alkaline phosphatase,total ATPase and Na^ -K^ -ATPase activities of plasma membrane were significantly decreased in both liver and kidney after chromium treatment.However,α-tocopherol (30mg/100g diet)supplementation can restrict the changes in these membrane-bound enzyme activities.Thus,the usefulness of dietary supplementation of α-tocopherol to restrain the chromium-induced membrane damage is suggested.     

Detection and occurrence of pentachlorophenol residues in chicken liver and fat

Abstract

A method for the detection of pentachlorophenol (PCP) residues in chicken liver and fat is presented. A detection limit of 0.002 mg/kg was achieved. Recoveries from liver and fat were in the range 82–88% and 95–97%, respectively.

Low level residues of PCP were found in all 1072 liver and 723 fat samples. These levels were <0.010 mg/kg in 92.7% of the fat and 75.6% of the livers. Only 0.75% of the liver samples had PCP levels>0.1 mg/kg. None of the more toxic impurities of PCP were detected in the chicken tissues.     

Assessment of thyroid hormone activity of halogenated bisphenol A using a yeast two-hybrid assay

The thyroid hormone agonist/antagonist activities of halogenated derivatives of bisphenol A (BPA) were assessed using a yeast two-hybrid assay incorporating the human thyroid hormone α (TRα), both with and without possible metabolic activation by rat liver S9 preparation. In the absence of the rat liver S9 preparation, 3,3′,5,5′-tetrabromobisphenol A (TBBPA), 3,3′,5,5′-tetrachlorobisphenol A (TCBPA), and 3,3′,5-trichlorobisphenol A (3,3′,5-triClBPA) exhibited agonist activity, whereas 3-chlorobisphenol A (3-ClBPA), 3,5-dichlorobisphenol A (3,5-diClBPA), 3,3′-dichlorobisphenol A (3,3′-diClBPA), and BPA did not. The activities of TBBPA and TCBPA increased markedly (7.6-fold and 3.1-fold, respectively) after their metabolic activation with the rat liver S9 preparation. TBBPA, TCBPA, and 3,3′,5-triClBPA inhibited the binding of triiodothyronine (T3) to TRα at 2 × 10⁻⁵ M without rat liver S9 treatment and 4 × 10⁻⁶ M with rat liver S9 treatment, demonstrating their T3 antagonist activity. These results revealed that metabolic activation by rat liver S9 significantly increased the agonist/antagonist potential of some halogenated BPAs.     

Antioxidant effect of L-cysteine on sodium-valproate-induced oxidative stress in rat liver: biochemical and ultrastructural approaches

L-Cysteine has protective efficacy in cases of oxidative tissue injury. Sodium valproate is widely used as an anticonvulsant and an antidepressant in spite of hepatotoxicity as side effect. The aim of this study was to evaluate the protective role of L-cysteine in liver toxicity induced by sodium valproate overdose. Release of the hepatic enzymes, aspartate aminotransferase and alanine aminotransferase, and levels of lipid profiles, as well as the oxidative, enzymatic, and non-enzymatic antioxidant were assessed. Liver damage was judged histologically. L-Cysteine decreased the activity of alanine aminotransferase and aspartate aminotransferase, as well as improved the level of lipid profile, increased the enzymatic antioxidant (catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase), and decreased the lipid peroxidation. L-Cysteine administration inhibited liver injury of sodium valproate.     

多氯联苯(PCBs)胁迫下鲫鱼肝脏EROD酶活性与血清性激素含量的相关性研究

以鲫鱼(Carassius auratus)为试验鱼类,研究其暴露于不同浓度的PCBs(多氯联苯)后鱼肝组织中EROD酶活性和血清性激素含量的动态变化,探讨了2者间的相关性。结果表明,鲫鱼在PCBs中暴露后,其肝脏组织中EROD酶被诱导,酶活性随PCBs浓度增大而增强,呈明显的剂量-效应关系;EROD酶活性随暴露时间延长而上升,10 d后达平衡;鲫鱼血清中睾酮含量随PCBs浓度增大和暴露时间延长呈下降趋势,但雌二醇含量则显著上升,表明PCBs对鱼类具有环境雌激素效应;在一定浓度范围内,EROD酶活性与血清睾酮含量呈负相关,与血清雌二醇含量呈正相关。因此可用鱼肝EROD酶和血清性激素含量的协同变化作为污染生物标志物来评价PCBs的早期污染生态效应。     

镉对鲫鱼鳃和肝脏超氧化物歧化酶活性的影响

使用浸浴法以 0 mg/ L、0 .73 mg/ L、1 .46 mg/ L、2 .95 mg/ L 4个镉 (Cd Cl2 · 2 .5H2 O)浓度为丰产鲫 (Carassiusauratus of Penze(♀ )× Cyprinusacutidorsalis(♂ ) )幼鱼染毒 ,测定了 1 4 4 h内鳃及肝组织中超氧化物歧化酶 (SOD)活性的变化。结果表明 ,低浓度组Cd曝露时 ,鲫鱼鳃和肝组织中 SOD活性的变化短时间内不明显 ,但随着处理时间的延长 ,Cd提高了鳃和肝组织中 SOD的活性 ,导致“毒物兴奋效应”。高浓度组 Cd曝露时均抑制了肝和鳃中的 SOD活性 ,其作用随着曝露时间的延长和浓度的升高而增强 ,SOD酶活性降低所造成的活性氧伤害是引起鲫幼鱼死亡的重要原因。肝组织中的 SOD酶活性和敏感性高于鳃 ,这与其执行的生理功能有关     

代谢活化作用对多溴代联苯类污染物类/抗甲状腺激素活性的影响

选用大鼠肝匀浆(S9)和鼠肝癌细胞(H4ⅡE)两种体系代谢活化多溴代联苯醚混标(BDEs)和十溴联苯醚(BDE209),采用重组甲状腺激素受体基因酵母检测BDEs和BDE209母体及其代谢产物的类/抗甲状腺激素效应.结果表明,BDEs和BDE209母体均不表现甲状腺激素效应(p>0.05);但是经S9和H4ⅡE细胞代谢活化后,其代谢产物表现出明显的类甲状腺激素活性和抗甲状腺激素活性(p<0.05),BDEs和BDE209的干扰甲状腺激素效应需要经过代谢活化步骤.比较不同代谢活化体系,重组酵母细胞本身的代谢活化作用并不显著,而H4ⅡE细胞和S9代谢活化体系均能够导致活性中间体.